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A closer look at a new 2026 literature review
For decades, the most polarizing question in Lyme medicine has not been whether people remain sick, but why. Patients live with persistent neurological, musculoskeletal, cognitive, and psychiatric symptoms long after an initial tick exposure. Clinicians see these patterns daily. Yet the dominant narrative has often insisted that active infection cannot persist once a short course of antibiotics has been completed.
A newly published 2026 review by Stricker, Fesler, and Johnson takes a sober, methodical look at that assumption—and quietly dismantles it.
Rather than arguing philosophy or policy, the authors do something refreshingly straightforward: they review the medical literature and ask a simple question. Has Borrelia burgdorferi ever been shown to persist in animals or humans after treatment, using direct detection methods?
The answer, based on their findings, is yes. Repeatedly.
Persistence isn’t a theory here—it’s been observed
This paper reviewed 56 studies—24 animal studies and 32 human studies—that used direct or functional testing to look for Borrelia after infection and, in many cases, after antibiotic therapy. These weren’t antibody tests or symptom questionnaires. They included culture, histology, xenodiagnosis, PCR, and in situ hybridization.
In other words, methods designed to answer one specific question: Is the organism still there?
Across these studies, Borrelia was detected months to years after infection, including after standard antibiotic treatment. Even more importantly, viable organisms—not just genetic fragments—were demonstrated in a significant number of both animal and human cases.
This matters, because much of the dismissal of persistent infection has hinged on the claim that there is “no credible scientific evidence” that Borrelia survives antibiotic therapy. That claim becomes difficult to maintain when live organisms are cultured, visualized in tissue, or transmitted through xenodiagnosis.
The monkey study that changed the conversation
One of the most compelling pieces of evidence discussed in this review comes from a rhesus macaque study by Embers and colleagues.
The design was intentional. The monkeys were treated with the same antibiotic regimen used in a landmark human trial often cited to argue against ongoing treatment: intravenous ceftriaxone followed by oral doxycycline.
The results were telling.
About 25% of the monkeys cleared the infection, demonstrating that antibiotics can work. But 75% did not. In those animals, Borrelia was later found in multiple tissues using culture, immunofluorescence, and PCR.
This nuance is critical. The question has never been whether antibiotics ever work. The real question is whether a subset of patients fails treatment because the organism persists in forms that are difficult to eradicate or detect.
This animal model suggests that they do.
The “debris” explanation falls short
Some researchers have proposed that ongoing symptoms are driven not by live infection, but by leftover bacterial debris that continues to provoke inflammation after the organism is dead.
That hypothesis sounds tidy—but it struggles to explain several observations.
DNA from dead bacteria is typically cleared rapidly from tissues. Multiple studies show this happens within hours to days. Yet in many of the studies reviewed here, Borrelia DNA, proteins, or whole organisms were found months or years later, sometimes in protected tissue sites, and sometimes capable of transmission.
Debris also cannot explain positive cultures, histologic identification of intact organisms, or xenodiagnosis showing viable transmission.
Inflammation may absolutely play a role. Immune dysregulation may persist. But these mechanisms are not mutually exclusive with ongoing infection—and the evidence suggests they often coexist.
Cysts, biofilms, and why detection is so difficult
The review also addresses something clinicians have long suspected but often struggle to explain to patients: Borrelia does not always exist in a form that standard antibiotics or standard tests are designed to address.
Under stress—including antibiotic pressure—Borrelia can shift into cell-wall deficient forms (often called L-forms or cysts) or embed itself within biofilms. These forms are metabolically quieter, more resistant to treatment, and far harder to culture or visualize.
This doesn’t make them imaginary. It makes them evasive.
Biofilms, in particular, can appear under microscopy as amorphous “debris,” which may explain why some studies dismissed what they were actually seeing. From a clinical perspective, this aligns with patients who partially improve, plateau, relapse, or respond only to layered or combination approaches over time.
Why this matters clinically
This paper does not argue that everyone with chronic symptoms has persistent infection. It does not claim that antibiotics are universally effective or appropriate. And it does not offer simple treatment answers.
What it does do is something far more important: it re-opens scientific space for honest inquiry.
When persistent infection is categorically denied, patients are often misdiagnosed, dismissed, or told their symptoms are “post-infectious” without further investigation. That leads to undertreatment, loss of trust, and prolonged suffering.
Recognizing that Borrelia can persist—sometimes despite treatment—doesn’t mandate one specific therapy. But it does mandate curiosity, humility, and individualized decision-making.
A broader frame
From a root-cause perspective, this fits what many of us see clinically. Chronic illness rarely arises from a single mechanism. Persistent microbes, immune dysregulation, inflammatory signaling, autonomic disruption, environmental exposures, and neuroimmune feedback loops often overlap.
This paper strengthens one critical piece of that puzzle: persistent Borrelia infection is biologically plausible, repeatedly observed, and clinically relevant in a subset of patients.
Ignoring that fact doesn’t resolve the controversy. It prolongs it.
The takeaway
The Lyme debate has never been helped by extremes. What moves the field forward is careful evidence, thoughtful interpretation, and willingness to sit with complexity.
This review doesn’t shout. It doesn’t sensationalize. It simply documents what has already been shown—again and again—when researchers actually look.
And sometimes, that’s exactly what science needs.